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Books on the topic 'Blood platelets Platelet activation'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Histophysiology of the circulating platelet. Springer-Verlag, 1990.

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2

1946-, Stute W., and Seminar on Empirical Processes (1985 : Düsseldorf, Germany), eds. Seminar on Empirical Processes. Birkhäuser Verlag, 1987.

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3

1947-, Kaplan-Gouet C., and Salmon Charles 1925-, eds. Platelet immunology. Karger, 1988.

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4

Guinivan, Phyllis. Platelet-derived growth factor (PDGF). U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1988.

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5

Wurzinger, Laurenz J. Histophysiology of the circulating platelet. Springer-Verlag, 1990.

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6

(Firm), Knovel, ed. Handbook of platelet physiology and pharmacology. Kluwer Academic, 1999.

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7

Platelet proteomics: Principles, analysis, and applications. John Wiley & Sons, 2011.

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8

F, Décary, and Rock G, eds. Platelet membrane in transfusion medicine. Karger, 1988.

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9

Johnson, Robert B. Storage of platelet concentrates following ultraviolet-B irradiation. s.n.], 1992.

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10

Canadian Workshop and Conference on Platelet Serology (1st 1985 Ottawa, Ont.). Platelet serology: Research progress and clinical implications. Edited by Décary F and Rock G. Karger, 1986.

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11

White, Melanie McCabe. Platelet protocols: Research and clinical laboratory procedures. Academic Press, 1999.

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12

1951-, Parnham Michael J., and Prop Gerrit, eds. Cologne Atherosclerosis Conference, Nr. 3, platelets. Birkhäuser, 1986.

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13

Gérard, Marguerie, Zwaal R. F. A, European Thrombosis Research Organisation, and Institut national de la santé et de la recherche médicale (France), eds. Biochemistry and physiopathology of platelet membrane =: Biochimie et physiopathologie de la membrane plaquettaire : proceedings of the Working Party on Platelet Membrane : Biochemistry and Physiopathology, held in Villard-de-Lans (France), 29-31 Januagy 1987. Libbey, 1988.

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14

Patrias, Karen. Platelet transfusion therapy: January 1981 through September 1986, 358 citations. U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.

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15

European Symposium on Platelet Immunology (1st 1990 Paris, France). Platelet immunology: Fundamental and clinical aspects : proceedings of the First European Symposium on Platelet Immunology held in Paris, Palais du Luxembourg (France), March 1-2, 1990 = Immunologie plaquettaire : aspects fondamentaux et cliniques. John Libbey Eurotext, 1991.

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16

1929-, Jamieson G. A., ed. Platelet membrane receptors: Molecular biology, immunology, biochemistry, and pathology : proceedings of the XIXth Annual Scientific Symposium of the American Red Cross held in Washington, DC, October 20-22, 1987. A.R. Liss, 1988.

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17

Working Party on Platelet Membrane: Biochemistry and Physicology (1987 Villard de Lans, France). Biochemistry and physiopathology of platelet membrane: Proceedings of the Working Party on Platelet Membrane, Biochemistry, and Physiopathology, held in Villard-de-Lans (France) 29-31 January 1987 = Biochimie et physiopathologie de la membrane plaquettaire. Editions INSERM, 1988.

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18

Murphy, Natalie P. Coronary thrombosis and thrombolysis: The role of platelet glycoprotein IIb/IIIa. University College Dublin, 1996.

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19

European Thrombosis Research Organisation. Workshop. Monoclonal antibodies and human blood platelets: Proceedings of the European Thrombosis Research Organisation Workshop, under the patronage of the Institut national de la santé et de la recherche médicale, held in Lyon (France), 26-27 September 1985. Edited by McGregor John Louis and Institut national de la santé et de la recherche médicale (France). Elsevier Science Publishers, 1986.

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20

Rhône-Poulenc Round Table Conference (4th 1985 Menthon-Saint-Bernard, France). Biology and pathology of platelet-vessel wall interactions: Proceedings of the Rhône-Poulenc Santé-INSERM Conference, held at Menthon-Saint-Bernard (Annecy), France, September 30th to October 2nd, 1985. Academic Press, 1986.

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21

Rhône-Poulenc Santé - INSERM Conference (1985 Menthon-Saint-Bernard). Biology and pathology of platelet-vessel wall interactions: Proceedings of the Rhône-Poulenc Santé - INSERM Conference, held at Menthon-Saint-Bernard (Annecy), France, September 30th to October 2nd, 1985. Academic Press, 1986.

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22

Cologne Atherosclerosis Conference (3rd 1986). Cologne Atherosclerosis Conference, No. 3, platelets: 3rd Cologne Atherosclerosis Conference, Cologne, April 23-25, 1986. Birkhäuser, 1986.

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23

1967-, Tsai Wei-Bor, ed. Biomaterials in blood-contacting devices: Complications and solutions. Nova Science Publishers, 2009.

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24

Antiplatelet therapy in ACS and A-Fib. Karger, 2012.

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25

Pharand, Chantal. The use of platelet glycoprotein IIB/IIIA receptor antagonists in the management of unstable angina and non-st-elevation myocardial infarction: A critical evaluation. s.n., 2000.

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26

Handbook of compounds with anti-inflammatory and anti-platelet aggregation activities isolated from plants. Nova Science Publishers, 2008.

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27

Platelet activation. Academic Press, 1987.

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28

S, Authi Kalwant, Watson Steve P, Kakkar V. V, and International Symposium on Mechanisms of Platelet Activation and Control, (1992 : London, England), eds. Mechanisms of platelet activation and control. Plenum Press, 1993.

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29

Curry, Nicola, and Raza Alikhan. Normal platelet function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0281.

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The platelet is a small (2–4 µm in diameter), discoid, anucleate cell that circulates in the blood. In health, it plays a vital role in haemostasis, and in disease it contributes to disorders of bleeding and thrombosis. Platelets are produced from the surface of megakaryocytes in the bone marrow, under tight homeostatic control regulated by the cytokine thrombopoietin. Platelets have a lifespan of approximately 7–10 days, and usually circulate in the blood stream in a quiescent state. Intact, undamaged vessel walls help to maintain platelets in this inactive state by releasing nitric oxide, which acts both to dilate the vessel wall and to inhibit platelet adhesion, activation, and aggregation. After trauma to the blood vessel wall, platelets are activated and, acting in concert with the endothelium and coagulation factors, form a stable clot. This chapter addresses platelet structure and function, and the response of platelets to vessel injury.

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30

1946-, Barnes Peter J., Page C. P, and Henson P. M. 1940-, eds. Platelet activating factor and human disease. Blackwell Scientific, 1989.

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31

A, FitzGerald G., Jennings Lisa K, Patrono Carlo 1944-, New York Academy of Sciences., and International Meeting on Platelets and Vascular Occlusion (3rd : 1993 : Santa Fe, N.M.), eds. Platelet-dependent vascular occlusion. New York Academy of Sciences, 1994.

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32

M, Winslow C., and Lee M. L, eds. New horizons in platelet activating factor research. Wiley, 1987.

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33

M, Winslow C., and Lee M. L, eds. New horizons in platelet activating factor research. Wiley, 1987.

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34

(Editor), C. P. Page, P. Barnes (Editor), and P. Henson (Editor), eds. Platelet Activating Factor & Human Disease, Frontiers in Pharmacology & Therapeutics. Blackwell Science, 1989.

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35

1946-, Barnes P. J., Page Clive P, and Henson P. M. 1940-, eds. Plateletactivating factor and human disease. Blackwell Scientific, 1989.

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36

S, Authi Kalwant, Bruchhausen F. von 1929-, and Walter U. 1949-, eds. Platelets and their factors. Springer, 1997.

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37

Platelet activating factor receptor: Signal mechanisms and molecular biology. CRC Press, 1993.

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38

1952-, Schmitz-Schumann M., Menz G, and Page C. P, eds. PAF, platelets, and asthma. Birkhäuser, 1987.

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39

Pruthi, Rajiv K. Coagulation (Hemostasis and Thrombosis). Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0295.

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The coagulation system has 2 essential functions: to maintain hemostasis and to prevent and limit thrombosis. The procoagulant component of the hemostatic system prevents and controls hemorrhage. Vascular injury results in activation of hemostasis, which consists of vasospasm, platelet plug formation (platelet activation, adhesion, and aggregation), and fibrin clot formation (by activation of coagulation factors in the procoagulant system). The anticoagulant system prevents excessive formation of blood clots, and the fibrinolytic system breaks down and remodels blood clots. Quantitative abnormalities (deficiencies) and qualitative abnormalities of platelets and coagulation factors lead to bleeding disorders, whereas deficiencies of the anticoagulant system are risk factors for thrombosis. Common disorders of hemostasis and thrombosis are reviewed.

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40

(Editor), J. Morley, ed. Paf in Asthma (Perspectives in Asthma Series, Vol 3). Academic Press, 1990.

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41

George, Holme, and Morley J, eds. PAF in asthma: Proceedings of a symposium held in Canada in June 1986. Academic Press, 1989.

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42

G, Holme, and Morley J. 1938-, eds. PAF in asthma. Academic Press, 1989.

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43

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.

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44

Kuiper, Gerhardus J. A. J. M., and Hugo ten Cate. Coagulation monitoring. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0266.

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Haemostasis is a dynamic process to stop bleeding after vessel wall damage. Platelets form a platelet plug via activation, adherence, and aggregation processes. The coagulation proteins are activated one-by-one, cascading towards fibrin polymerization, a process controlled by thrombin generation. Fibrinolysis is the process responsible for fibrin mesh degradation, which is also controlled by thrombin. Besides procoagulant proteins, anticoagulant proteins maintain a balance in the haemostatic system. Measuring platelet count and function can be done as part of the monitoring of haemostasis, while coagulation times are measured to assess the coagulation proteins. Degradation products of fibrin and lysis times give information about fibrinolysis. Point-of-care monitoring provides simple, rapid bedside testing for platelets and for whole blood using viscoelasticity properties. In trauma-induced coagulopathy (TIC) platelet counts and coagulation times are still common practice to evaluate haemostasis, but point-of-care measurements are being used more and more. Medication interfering with haemostasis is frequently used in intensive care unit patients. Each (group of) drug(s) has its own monitoring tests either based on classical or novel techniques.

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45

Michelson, Alan D. Platelets. 2nd ed. Academic Press, 2006.

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46

D, Michelson Alan, ed. Platelets. 2nd ed. Academic Press/Elsevier, 2007.

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47

D, Michelson Alan, ed. Platelets. Academic Press, 2002.

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48

Platelets. Elsevier Science & Technology Books, 2012.

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49

(Editor), J. Seghatchian, E. L. Snyder (Editor), and P. Krailadsiri (Editor), eds. Platelet Therapy. Elsevier, 2000.

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50

1947-, Kurtz Sanford R., Brubaker Daniel B, and American Association of Blood Banks., eds. Clinical decisions in platelet therapy. American Association of Blood Banks, 1992.

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